Evidence map›Paper›PMID 29434213›Full record

ArticleCell death & disease2018

Autophagy mediates glucose starvation-induced glioblastoma cell quiescence and chemoresistance through coordinating cell metabolism, cell cycle, and survival.

Lian Wang, Zhouchun Shang, Yang Zhou, Xinyu Hu, Yihong Chen, Yantao Fan, Xiaoyu Wei, Liang Wu, Qiujuan Liang, Jun Zhang and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
5.2field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

44 citing papers in PubMed, 73 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. Dietary methionine restriction in cancer development and antitumor immunity.Trends in endocrinology and metabolism: TEM · 2024
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 4 institutions in 1 country.

Lian WangShanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China.
Zhouchun ShangShanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China.
Yang ZhouDepartment of Regenerative Medicine, Tongji University School of Medicine, Shanghai, 200092, China.
Xinyu HuShanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China.
Yihong ChenDepartment of Cardiology, Shanghai Changzheng Hospital Second Military Medical University, Shanghai, China.
Yantao FanShanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China.
Xiaoyu WeiBGI-Shenzhen, Shenzhen, China.
Liang WuBGI-Shenzhen, Shenzhen, China.
Qiujuan LiangShanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China. qiujuan_liang@tongji.edu.cn.
Jun ZhangDepartment of Regenerative Medicine, Tongji University School of Medicine, Shanghai, 200092, China. junzhang@tongji.edu.cn.
Zhengliang GaoShanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China. zhengliang_gao@tongji.edu.cn.
Tongji University · CNBGI Group (China) · CNShanghai Tenth People's Hospital · CNSecond Military Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolic reprogramming is pivotal to sustain cancer growth and progression. As such dietary restriction therapy represents a promising approach to starve and treat cancers. Nonetheless, tumors are dynamic and heterogeneous populations of cells with metabolic activities modulated by spatial and temporal contexts. Autophagy is a major pathway controlling cell metabolism. It can downregulate cell metabolism, leading to cancer cell quiescence, survival, and chemoresistance. To understand treatment dynamics and provide rationales for better future therapeutic strategies, we investigated whether and how autophagy is involved in the chemo-cytotoxicity and -resistance using two commonly used human glioblastoma (GBM) cell lines U87 and U251 together with primary cancer cells from the GBM patients. Our results suggest that autophagy mediates chemoresistance through reprogramming cancer cell metabolism and promoting quiescence and survival. Further unbiased transcriptome profiling identified a number of clinically relevant pathways and genes, strongly correlated with TCGA data. Our analyses have not only reported many well-known tumor players, but also uncovered a number of genes that were not previously implicated in cancers and/or GBM. The known functions of these genes are highly suggestive. It would be of high interest to investigate their potential involvement in GBM tumorigenesis, progression, and/or drug resistance. Taken together, our results suggest that autophagy inhibition could be a viable approach to aid GBM chemotherapy and combat drug resistance.

Indexed as

AutophagyCell CycleDrug Resistance, NeoplasmCell Line, TumorCell SurvivalGlioblastomaGlucoseHumansGlucose

Identifiers

PMID29434213
PMCPMC5833690
OpenAlexW2789611666

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.